Acinetobacter is a genus of gram-negative bacteria that includes opportunistic pathogens. The most clinically important species are A. baumannii and A. lwoffii. A. baumannii is commonly found in hospitals and can cause infections in immunocompromised patients. It is able to survive on surfaces and in the environment. Treatment is challenging due to high levels of antibiotic resistance, though carbapenems and polymyxins may be used. Proper hygiene and cleaning can reduce transmission in clinical settings.
2. Introduction
The name, Acinetobacter, comes from the
Latin word for "motionless," because
they lack cilia or flagella with which to
move.
Have 32 species, A. baumanii and A.
lwoffii have greatest clinical importance.
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3. Introduction
Most species are not significant sources of
infection. However, one opportunistic
species, Acinetobacter baumannii, is
found primarily in hospitals and poses a
risk to people who have supressed
immunity.
>2/3 of Acinetobacter infections are due to
A. baumannii
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6. Epidemiology
In the hospital
Environmental surface
Ventilators, dialysis machines, air ventilation
systems, water sources
Hands
Contaminated suction equipment
Respiratory, urinary, GI tracts & wounds of
patients
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9. Biochemical Profile
Both A.baumennii and
A.lwofii are Catalase
positive and Oxidase
Negative.
A.baumennii ferment
glucose, xylose and
lactose but A.lwofii
cannot ferment.
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10. Rapid Detection
Rapid detection of Acinetobacter can be
done by RapID ONE Panel (remel) and
Api 20 E strips. These can differentiate up
to species level.
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11. Molecular Detection
A.baumennii and A.lwofii can be detected
by PCR.
recA specific primers are used to detect
recA gene in A.baumennii, giving a 382 bp
fragment
est specific primers are used to detect est
gene in A.lwofii, giving a 309 bp product.
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12. Pathogenesis
Opportunistic pathogen
Survive under dry conditions
Virulence Factors
Polysaccharide capsule, prevent complement
activation, delay phagocytosis
Fimbriae (adhere to human bronchial epithelium)
Pilli (colonization of environmental surface to form
biofilms)
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13. Transmission
Acinetobacter can
be spread from
person to person
(infected or
colonized patients),
contact with
contaminated
surfaces of exposure
to the environment.
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14. Antibiotic Resistance
Acinetobacter species
are capable of
accumulating multiple
antibiotic resistance
genes, leading to the
development of
multidrug-resistant or
even panresistant
strains.
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15. Antibiotic Resistance
Mechanisms
Antibiotic-altering enzymes (beta-lactams,
carbapenems, aminoglycosides)
Reduced outer membrane porin expression
(beta-lactams, carbapenems)
Altered penicillin-binding proteins (beta-
lactams, carbapenems)
DNA gyrase and topoisomerase IV
mutations (quinolones)
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16. Treatment
Multidrug-resistant A. baumannii is a
common problem in many hospitals. First
line treatment is with a Carbapenems
antibiotic such as imipenem, but
carbapenem resistance is increasingly
common. Other treatment options include
Polymyxin, Tigecycline and
Aminoglycosides.
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17. Treating the Resistant Infections
Colistin and Polymyxin B have been used
to treat highly resistant Acinetobacter
infections. The choice of appropriate
therapy is further complicated by the
toxicity of colistin which is mainly renal.
Acinetobacter isolates resistant to colistin
and Polymyxin B have also been reported
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18. Summary
Opportunistic pathogen
Nosocomial infection
Grow best at aerobic conditions
Can be transmitted by contact
Possessing antibiotic resistant
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#5: Short, broad rod during rapid growth
Coccobacillary shape in stationary phase
#9: Colonies are 1 to 2 mm, nonpigmented, domed, and muciod, with smooth to pitted surfaces.
#10: Oxidase negative (opposite to Neisseria spp. or Moraxella spp.)
Haemolytic
Indole negative.
Catalase positive.
#16: Quinoloine and nalidixic acid- inhibit DNA/RNA synthesis
Rifamycine- prevent DNA synthesis
Erythromycine, chloramphenicol- disruption of 50s subunit of ribosome
Tetracycline, gentamycine and streptomycine- 30s subunit disruption
#17: Polymyxin- Disruption of cell membrane
Penicilline, cephalosporine and beta-lactam - inhibition of cell wall synthesis
Sulfonamide and trimethoporine- inhibition of folic acid synthesis